Fig. 5: Myeloid cell-specific ITGA5 loss reduces microvascular density and perturbs formation of coated mature vessels in the healing infarct.

A CD31 immunohistochemistry was used to label endothelial cells. Representative images show CD31 staining of the infarcted area, border zone and remote remodeling myocardium from ITGA5 fl/fl and Myα5KO mice after 7 and 28 days of coronary occlusion. The arrow identifies a typical CD31+ microvessel. Quantitative analysis showed that Myα5KO mice have significantly reduced microvascular density in the infarct zone at the 7-day timepoint (B), and in the border zone (C) after 28 days of coronary occlusion. Microvascular density in the remote remodeling myocardium was comparable between Myα5KO mice and corresponding ITGA5 fl/fl controls (D) (**p < 0.01, ***p < 0.001, ITGA5 fl/fl 7d: n = 14, Myα5KO 7d: n = 12, ITGA5 fl/fl 28d: n = 13, Myα5KO 28d: n = 13 biologically independent experiments). Scalebar = 100um. E In healing infarcts, microvessels undergo maturation acquiring a coat comprised of α-SMA-expressing mural cells (arrowheads). Representative images show α-SMA immunofluorescence staining of infarcted and remote areas from ITGA5 fl/fl and Myα5KO mice after 7 and 28 days of coronary occlusion. The arrow identifies a typical α-SMA+ vessel. Myα5KO mice had significantly reduced density of mature α-SMA+ microvessels in the infarct zone at the 28-day timepoint (F). The density of α-SMA+ vessels in the remote remodeling myocardium was comparable between Myα5KO and ITGA5 fl/fl mice (G). (****p < 0.0001, ITGA5 fl/fl 7d: n = 14, Myα5KO 7d: n = 12, ITGA5 fl/fl 28d: n = 13, Myα5KO 28d: n = 13 biologically independent experiments). Data are shown as mean values +/- SEM. Statistical analysis was performed using one-way ANOVA, followed by Sidak post-hoc test. Source data are provided as a Source Data file. Scalebar = 100um. I infarct area, R remote area.